I. Introduction
Every 21 Seconds, One Person In The United States Suffers A Traumatic Brain Injury Trauma is the leading cause of death and disability among Americans less than 44 years of age, and is the fourth leading cause of death overall (Appendix 1). Most trauma deaths are due to brain injury. Traumatic Brain Injury (TBI) – Incidence Causes and Outcome The CDC estimates that annually, over one million Americans seek medical attention for head trauma1, nearly 230,000 are admitted to hospitals2 and 50,000 die3. Using 1995-1996 preliminary hospitalization and mortality data from 12 states (Alaska, Arizona, Sacramento County [California], Colorado, Louisiana, Maryland, Missouri, New York, Oklahoma, Rhode Island, South Carolina, and Utah), the CDC estimates that the average TBI incidence rate (combined hospitalization and mortality rate) is 95 per 100,000 population. Traumatic brain injury is most prevalent among adolescents, young adults, and people older than 75 years of age. In all age groups, the risk of TBI among males is twice the risk among females. The leading causes of TBI are motor vehicle accidents, violence, and falls with nearly two-thirds of firearm-related TBI's thought to be self-inflicted. Causes vary by age with falls leading among persons over the age of 65 and transportation among persons aged 5 to 64 years.

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Nationally, there was a 22% decline in the TBI-related death rate from 24.6/100,000 U.S. residents in 1979 to 19.3/100,000 in 1992.20 Firearm-related rates increased 13% from 1984 through 1992, undermining a 25% decline in motor vehicle-related rates for the same period. Firearms surpassed motor vehicles as the largest single cause of death associated with traumatic brain injury in the United States in 1990. These data highlight the success of efforts to prevent traumatic brain injury due to motor vehicles and failure to prevent such injuries due to firearms.

Overall mortality for TBI is approximately 22%, though outcome varies greatly depending on the cause: 91% of firearm-related TBI’s result in death whereas only 11% of fall-related TBI’s are fatal. TBI-related disability Based on national TBI incidence data and data from the Colorado Traumatic Brain Injury Registry the CDC estimates that, annually, more than 80,000 Americans are discharged from hospitals with TBI-related disabilities and that 5.3 million Americans are living today with a TBI-related disability5. Neurological impairments following TBI include coma, paralysis, speech and swallowing difficulties, emotional problems, memory difficulties and seizures. The severity varies, but many patients remain permanently disabled requiring long-term nursing care and remaining at high risk for medical complications such as pneumonia, urinary tract infections, skin ulcers, pressure sores, muscle wasting and frozen joints.

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Cost to Society Though the economic impact of TBI may be estimated, the cost to society in terms of physical and emotional toll for patients and their families is incalculable. Nevertheless, attempts have been made to quantify this cost. One study estimated that the annual economic burden of TBI in the United States was approximately $37.8 billion in 1985.5 This estimate included $4.5 billion in direct expenditures for hospital care, extended care, and other medical care and services; $20.6 billion in injury-related work loss and disability; and $12.7 billion in lost income from premature death. SFGH TBI Initiative (SFGH/TBII) San Francisco General Hospital is the only Level-I Trauma center in the San Francisco Peninsula – receiving all trauma patients from the City and County of San Francisco as well as Northern San Mateo County and parts of Marin County. Severe trauma admissions at SFGH total 1200/year with 350-400 of these involving head injuries. In an ongoing effort to provide high-end, state-of-the-art Neurotrauma care, the SFGH/TBII provides a framework for the development of comprehensive multidisciplinary TBI treatment guidelines spanning from the pre-hospital setting, through the Emergency Department, Intensive Care Unit, and acute care floor, and culminating in programs focused on neurological recovery. The goal is to maximize return of neurological function and to provide avenues for community re-integration through intensive rehabilitation and vocational re-training (where possible) – and in the process, to instill in our patients a sense of purpose, pride, self-esteem and confidence. The SFGH/TBII also provides an infrastructure for the development of clinical research programs aimed at critically assessing current clinical practices and developing cutting-edge treatment protocols for TBI patients. The final mission of the SFGH/TBII is to develop educational programs for patients, their families, the community at large and health-care professionals. These may take the form of safety education and prevention programs for elementary school, junior and high school students or educational materials such as literature and videos for patients and their families. Educational programs for health-care professionals include regularly scheduled TBI in-service at SFGH as well as continuing medical education courses within the UCSF/SFGH community. The educational process naturally extends to presentations at national and international neuroscience conferences, and mainly focuses on research-related activities. The following SFGH/TBII document intended to be comprehensive yet flexible, designed as a “work-in-progress”, and intended to be modified as our knowledge if TBI improves. It was created with input and support from anesthesia, critical care 6

II. Critical and Acute Care Management of TBI
Background Trauma is the leading cause of death and disability among Americans less than 45 years of age, and is the fourth leading cause of death overall (Appendix 1). The most common cause of death within this group is brain injury. Severe brain injury is defined as head trauma resulting in an admission Glasgow Coma Scale score of 3-8. Traumatic brain injury (TBI) results in an alteration of cerebral physiology which may be amenable to interventions directed at limiting the injury cascade and, therefore, secondary injury. It has been recognized that, both nationally and locally, approaches to the management of the head injured patient vary significantly. This has led to the formation of evidence-based Guidelines for the Management of Severe Head Injury, which were published by the Brain Trauma Foundation in 19952 and revised in 20002. Purpose • • The purpose of this document is to provide standardized guidelines for the critical care management of the head injured patient at San Francisco General Hospital. These guidelines are based generally on the Guidelines for the Management of Severe Head Injury, which were published by the Brain Trauma Foundation in 1995 and revised in 2000. They have been modified and expanded to address issues specific to San Francisco General Hospital and reflect approaches to certain issues not addressed in the Guidelines for the Management of Severe Head Injury. These guidelines do not replace the physician’s judgment in individual cases, but may be considered reasonable and current approaches to the management of the critically ill adult head injury patient. While this document does not address specific guidelines for the management of pediatric head injury patients, many of the same principles are applicable. These guidelines are intended to foster a coordinated, cooperative environment among the multidisciplinary team caring for head injured patients, which includes, but is not limited to, the Neurosurgery and Neurology Services, the Critical Care Service, the Trauma Surgery Service, Critical Care Nursing and Rehabilitation and Social Services.

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Assessment Background Performance of serial neurological examinations by the interdisciplinary team is an essential component in the care of traumaticaly brain injured patients. Serial examination allows for detection of not only drastic but subtle changes in neurological status thus, allowing for prompt intervention to prevent further neurological disability and possibly death. Glasgow Coma Score The Glasgow Coma Scale was designed to meet a need for rapid and repetitive assessment of the head injured patient. The scale is used to assess coma and impaired consciousness in the patient suffering from a brain injury. The scale assesses three components; eye opening, verbal response and motor response. The examiner should note the BEST score in all areas of testing. (See Appendix C-1) Orientation Orientation assessment is reflective of cognitive impairment. The statement A & O X3 does not imply performance of an appropriate exam. It fails to identify specific components which may influence cognitive interventions. Components of a complete orientation exam: Person (First and Last name) Place (Hospital, City, State) Date (Year, Month, Day) If the patient is unable to appropriately respond, the examiner should rule out the possibility of aphasia. A quick assessment tool to use is to have the patient repeat the following sentence (No if ands or buts). An inability to accurately repeat this statement implies the presence of an aphasia and requires detailed work-up by Speech Therapy. (See Cognition and Behavioral Guidelines) Motor When assessing the motor response of a head injured patient it is imperative that a detailed exam be performed. If the patient is cooperative motor strength should be tested in all four extremities with comparisons made bilaterally.

Goal • Performance of a complete neurological examination in order to rapidly detect deviations from baseline thus preventing neurological disability.

Guidelines 1. 2. 3. 4. Perform routine serial neurological examinations every 2-4 hours as appropriate. MD notification of subtle or major neurological changes from baseline. Repeat Head CT for changes in neurological status, as indicated. Neurosurgical intervention as appropriate based upon findings.

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General Critical Care Issues Background Patients with severe head injury are critically ill and therefore have multiple issues related to general critical care management. These include, but are not limited to, nutritional support, prevention of deep venous thrombosis and gastrointestinal ulcers, and routine issues of IV fluid and blood product management. Goals • • • Prevent complications of critical illnesses that may affect severe head injury patients. Ensure adequate nutrition in critically ill head injury patients.

Guidelines 1. Nutritional Support (please see nutritional guidelines) • Enteral feeding will commence as early as feasible, preferably within 24 hours post-trauma. 140% of resting metabolism for most patients; 100% of resting metabolism for patients receiving neuromuscular blockade. • Duodenal feedings are preferred over stomach feedings. • For patients who cannot receive enteral feeding, TPN will be provided. • Upon initiation of TPN or enteral feeding the maintenance IVF rate. • will be decreased, in an effort to maintain a total intake balance. • appropriate to the patient’s fluid status. 2. DVT Prophylaxis • Sequential compression devices (SCDs) will be the preferred method of DVT prophylaxis and will be initiated, if possible based on other injuries, at time of admission and will be maintained until the patient is ambulatory. • No pharmacological prophylaxis will be used during the first 7 days following severe TBI or multi-trauma with any intracranial bleeding. • At least one post-injury or post-operative CT Scan must confirm not extension of intracranial hemorrhage prior to initiation of pharmacological DVT prophylaxis. • Pharmacological prophylaxis will consist of Enoxaparin 40mg SQ daily or weight adjusted doses of heparin SQ. • In any patient who has undergone craniotomy or craniectomy, no pharmacological prophylaxis will be started before post-operative day 7 of the most recent neurosurgical operation, and then only at the discretion of the Attending Neurosurgeon. • No pharmacological prophylaxis will be used within 48 hours of insertion of removal of any intracranial monitoring device. • The Attending Neurosurgeon may elect not to initiate pharmacological prophylaxis on post-injury day 7 in select cases. 3. Ulcer Prophylaxis • An H2-blocker (e.g. famotidine) will be initiated at time of admission. • Sucralfate or omeprazole are alternatives. 13

4. IV Fluids • All infusions will be mixed in 0.9% NS. • Plasmalyte is an alternative IV fluid, especially in patients with metabolic acidosis. • Fluid balance will be assessed every 12 hours; the physician will be notified if the fluid balance is 500 ml greater or negative. • Hyponatremia will be aggressively avoided and treated. o For Na < 135, salt tablets and/or 3% NaCl administration will be considered. o Fluid restriction will not be undertaken, as hypovolemia is to be avoided in patients with severe head injury. 5. Hematology • DIC may occur in the setting of severe head injury. • In the absence of bleeding, CBC/plts, PT/PTT will be checked daily. • INR will be maintained < 1.4. • Platelet count will maintained above 100,000 at the discretion of the Neurosurgery Attending. • RBC transfusion will be considered for hematocrit < 30%, even in the absence of DIC.

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Initial Resuscitation of Blood Pressure and Oxygen Background In head injured patients, both hypotension (defined as a systolic BP < 90 mmHg) and hypoxia (defined as apnea, cyanosis, or a PaO2 < 60 mmHg) are associated with worsened clinical outcome.4 This occurs presumably because hypotension and hypoxia cause secondary injury in vulnerable brain tissue. While these insults may occur at any point in the clinical course of a patient with head injury, they often occur in the pre-hospital setting or during Emergency Department (ED) resuscitation. Patients with severe TBI may mask hypovolemic hypotension because of the Cushing’s response to intracranial hypertension. As such, patients may benefit from central venous monitoring during the period of acute fluid resuscitation to adequately assess their intravascular volume. A gradual increase in blood pressure associated with a gradual decrease in pulse (even if both are within normal limits) should suggest the development or progression in intracranial hypertension. Goals • • • Closely monitor patient for evidence of either hypotension or hypoxia. Promptly and aggressively treat hypotension and hypoxia. Minimize exposure of vulnerable brain tissue to secondary injury.

Guidelines 1. Hemodynamic resuscitation should begin in the ED with the placement of two large-bore (14 or 16 G) IV’s when possible. A groin Cordis may be placed in lieu of a peripheral IV. 2. A subclavian central line should be placed when possible for volume-status assessment. The groin Cordis may be used to place a long central venous pressure line as long as two large-bore IV’s are available for fluid resuscitation. Internal jugular lines are not practical in the ED setting since most patients will be wearing cervical collars. 3. A temperature-sensing Foley catheter should be inserted during the initial resuscitation. This will help assess the patients fluid status as well as core body temperature. 4. Systemic blood pressure should be recorded every five minutes during the initial resuscitation (ED) via automated sphygmomanometer. An arterial bloodpressure catheter (radial) should be placed as soon as possible to allow for continuous blood pressure readings. This procedure should be performed by a senior-level resident or an attending to ensure efficiency. 5. Volume resuscitation with 0.9%NS or blood (when appropriate) is the first intervention. Plasmalyte may be considered as an alternative resuscitation fluid, especially in patients with metabolic acidosis. 6. Strict avoidance of hypotonic (0.45% and 0.225% NaCl) and D5-containing solutions should be observed during acute resuscitation and as routine maintenance fluids in the intensive care unit (ICU). 15

7. At a minimum, systolic BP should be maintained above 90 mmHg. Ideally, mean arterial pressure (MAP) will be maintained above 90 mmHg, since a systolic blood pressure of 90 mmHg may be inadequate in the setting of elevated ICP. 8. Systemic hypertension generally should not be treated in the acute setting of TBI, since this may reflect the body’s natural response to intracranial hypertension. 9. Antihypertensive medications may be administered if the systolic blood pressure is greater than 220 mm Hg. Beta blockers are the drug of choice in the absence of bradycardia. Calcium channel blockers or nitrates may be used as well, though the latter may theoretically increase ICP by causing cerebral vasodilation. Hydralazine should be avoided since it is thought to uncouple cerebral blood flow from metabolism. 10. Pressors may be necessary in addition to volume resuscitation, especially in the setting of acute spinal cord injury (SCI). Epinephrine, Dopamine or Neosynephrine are the pressors of choice. Neosynephrine may induce bradycardia in SCI and is generally reserved for use in TBI. The use of pressors in the acute setting should be agreed upon by ED, Trauma, Anesthesia and Neurosurgery attendings as applicable. 11. Early intubation may be necessary to avoid hypoxemia in patients with severe head injury. While there is theoretical concern about pulmonary oxygen toxicity in patients receiving an FiO2 > 0.6, concerns of systemic and cerebral hypoxia take precedence. 12. Treatment with supplemental oxygen will be initiated in the Field and continued after arrival to ED. 100% O2 will be given prior to intubation and continued during the initial post-intubation period. FiO2 will be adjusted according to the the postintubation arterial blood gas (ABG). 13. Rapid-sequence induction (RSI) should be carried out using Etomidate (0.1-0.3 mg/kg) and succinyl choline or Rocuronium as the agents of choice. Succinylcholine may theoretically increase ICP by depolarizing skeletal muscle, though patient outcome is unlikely affected by its use. Rocuronium, on the other hand is longer acting than succinealcholine – a concern if intubation is not readily accomplished. Furthermore, it prevents the neurological examination of patients for a longer time than succinealcholine. Rocuronium may be reversed after 2030 minutes with Neostigmine (20-70 mcg/kg) and glycopyrolate (0.6 mcg/kg). 14. Ventilation rate should be controlled to maintain adequate oxygenation. Because of the significant effects of ventilation on cerebral blood flow, hyperventilation during the acute resuscitation should be reserved only for patients with evidence of acute brain herniation. Hyperventilation can also decrease venous return, cardiac output, and blood pressure, thereby increasing the incidence of secondary brain injury. 15. Barbiturates and Propofol – while neuroportective – should be avoided because they can cause hypotension. 16. Initial serological studies must include the following • Post-resuscitation Arterial Blood Gas • Chem-10 and Serum Osmolarity • CBC with platelets • Coagulation panel (PT/PTT/INR) • Type and Screen (cross # of units as necessary) • Urine toxicology 16

Mechanical Ventilation Background Immediately following injury, cerebral metabolic demands for both oxygen and glucose increase dramatically. Unfortunately, the risk of both hypoxia (defined as a PaO2 of < 90mmHg) and hypoventilation (and subsequent hypercapnea) is highest during this very same period of time. The principle purpose of mechanical ventilation in severe head injury is to ensure adequate systemic and cerebral oxygenation. Airway control through the use of endotracheal intubation also prevents both upper airway obstruction and aspiration. Mechanical ventilation has the additional benefit of aiding in intracranial pressure (ICP) management. In the past, aggressive hyperventilation had been a cornerstone of head injury management because of the ability to decrease ICP by decreasing cerebral blood volume via hypocapnic cerebral vasoconstriction. Recent evidence has demonstrated, however, that aggressive prophylactic hyperventilation actually worsens outcome following severe head trauma9. The presumed mechanism for this is exacerbation of cerebral ischemia from the hypocapnic vasoconstriction. Although some difference of opinion exists, hyperventilation is best suited for a short-term strategy for lowering ICP until other measures can be instituted and should be avoided as a long-term intervention. Goals • • Ensure adequate oxygenation, ventilation, and airway protection. Aid in short-term control of elevated ICP while avoiding secondary brain injury from hypocapnic vasoconstriction-induced cerebral ischemia.

Guidelines 1. Quick assessment for symptoms/signs of hypoxia: • Cyanosis • Tachycardia/dysrhythmias • Hypercapnea • Hypoxia • Anxiety/restlessness/irritability • Somnolence/confusion/decreased mental acuity • Dyspnea 2. Modes and Methods of Mechanical Ventilation • The initial goal in all patients will be normoventilation, recognizing that pH defines ventilatory status, as driven by the medulla1. In patients with normal lungs, a normal ABG is 7.40/40/100. A CO2 of 35 in these patients represents mild hyperventilation. In patients with metabolic acidosis or alkalosis or baseline respiratory alkalosis, there is insufficient current knowledge in the absence of CBF monitoring to know how CBF is affected. Thus, a normal pH will be the goal of ventilation.

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• • • • •

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Initial ventilator settings will involve volume-controlled ventilation (AC or SIMV) with PEEP of 5. Recognizing that patients set their own minute ventilation via their medullary respiratory drive, patients that hyperventilate themselves (neurogenic hyperventilation) will be allowed to do so as changing mode of ventilation will not affect this and it is currently unclear if neurogenic hyperventilation is deleterious or compensatory. A goal PaO2 of 100 mmHg will be maintained. PEEP of < 10 cm H2O will be tolerated without concern for exacerbation of ICP. On a patient-by-patient basis, the effect of PEEP on ICP will be considered. Please see section III on initial resuscitation for reference to Rapid-sequence induction (RSI). Because ventilation is a primary ICP-management modality, all changes in ventilation parameters in patients with ICP monitors must be cleared by the neurosurgery Chief Resident or Attending. Hyperventilation o Prophylactic hyperventilation will not be instituted o Hyperventilation may be used as an acute strategy to lower ICP in patients with evidence of acute brain herniation while the patient is being transported to CT, OR, or other interventions such as ventriculostomy placement are being instituted. o Hyperventilation using manual bagging may be more immediately effective than just changing ventilator settings. o End-tidal CO2 (ETCO2) will be monitored in all patients with an ICP monitor. The goal ETCO2 is 1-5 points below pCO2 as determined by correlating the patient’s ABG to ETCO2. o All ED patients suspected of having a brain injury should have ETCO2 monitoring as soon as possible after intubation. ETCO2 monitoring should also be carried out during transport from the ED, during radiographic evaluation (CT, IR) and during transport to the OR or ICU. This is done to prevent over-hyperventilation. o After hyperventilation has been used, it will be withdrawn slowly in a stepwise fashion over 2-4 hours to avoid rebound in ICP. Tracheostomy o Controversy exists regarding the timing of tracheostomy after severe head injury. o In general, tracheostomy will be considered when a patient has been intubated for 24 days and extubation is not deemed to be imminent. o Early tracheostomy (prior to 14 days) may be considered in patients with the likely need for long-term mechanical ventilation or airway protection.

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Intracranial Hypertension Background Intracranial pressure (ICP) is frequently elevated in patients with severe head injury. This results from the fact that while skull volume is fixed, intracranial mass volumes – brain parenchyma, blood and cerebrospinal fluid (CSF) – are variable. As such, a volume increase in any one of these components will lead to an increase in intracranial pressure (ICP). Cerebral edema, presence of an intracranial hematoma, and hydrocephalus may all cause intracranial hypertension. The aim of ICP control, therefore, is to decrease the intracranial volume of any one, two or all three components. This goal can be attained through both surgical and non-surgical means, and treatment decisions balance the risks and benefits of each compared to the other. Because of ethical considerations, no prospective randomized controlled trials have been conducted addressing whether treatment of elevated ICP improves outcome from severe head injury. However, a large body of evidence exists suggesting that ICP monitoring and management do, in fact, impact outcome following head injury. Normal ICP is below 10 mmHg; sustained ICP above 20 mmHg6 is concerning and should probably be treated. Goals • • • • Detect early elevations in ICP. Promptly treat intracranial hypertension Maintain ideal cerebral perfusion pressure (CPP). Minimize exposure of vulnerable brain tissue to secondary injury.

Guidelines 1. Indications for ICP Monitoring • ICP monitoring is appropriate for all patients with severe head injury (GCS 38) with an abnormal admission head CT scan. • ICP monitoring is appropriate for all patients with severe head injury (GCS 38) with a normal head CT scan if two or more of the following are present: o age > 40 o unilateral or bilateral motor posturing o systolic blood pressure < 90 mmHg • ICP monitoring may also be considered in patients with head injury who are undergoing non-neurosurgical operative procedures early in their hospital course, during which time neurologic examination will be unavailable. 2. Technology for ICP Monitoring • Placement of a ventricular catheter is the preferred method for ICP monitoring as it allows CSF drainage for the treatment of elevated ICP. • When placement of a ventricular catheter is not deemed appropriate (i.e. slit ventricles, coagulopathy with INR > 1.7 or platelet count < 50,000), then use 19

Guidelines 1. CPP Management • A CPP of > 60 mmHg will be maintained using volume and pressors as necessary. • Threshold CPP will be tailored to individual patients using cerebral monitoring tools such as ICP, TCD, jugular venous oxygen saturation (SJVO2), and EEG. 2. Hemodynamic Monitoring • Insufficient evidence exists currently to recommend one method of hemodynamic monitoring in the head injured patient over another. Therefore, we will recommend that all patients undergoing ICP monitoring receive a central venous catheter (CVP) preferably via a subclavian route (to avoid possible IJ thrombosis, carotid artery puncture, and to reserve the IJ for SJVO2 monitoring). • Patients will also receive an arterial catheter, preferably at the radial site. By convention, the arterial pressure transducer will be placed at the level of the right atrium. This acknowledges that some published protocols have used arterial pressures at the level of the cerebral ventricles for CPP calculations. • In order to minimize the effect of head-of-bed (HOB) elevation on CPP, HOB should be raised no more than 25o. This strategy also addresses the observation that cerebral blood flow drops as the HOB elevation exceeds 30o – even in the setting of a constant CPP, and with the a-line zeroed at the Foramen of Monroe. • Pulmonary artery catheters will be used at the discretion of the treating physician, particularly in patients who cannot be managed via other methods (CVP line, clinical evaluation, cardiac echo). 21

3. Pressor and Volume Therapy • CVP will be maintained at 5-8 mmHg, which is slightly hypervolemic. If a PA catheter is used, then PCWP will be maintained at 8-12 mmHg. Because these pressure measurements may be altered by changes in intrathoracic pressure which accompany PEEP, ARDS/lung injury, and increased intraabdominal pressure, attention must be made to correlate intravascular pressures with other measures of volume status such as urine output and heart rate in order to ensure euvolemia or slight hypervolemia. • When pressors are used for CPP management, attention will be made to ensure that the patient is adequately fluid resuscitated before instituting a pressor infusion. Initial pressor of choice is phenylephrine (5-400 mcg/min), with dopamine (5-20 mcg/kg/min) an alternative choice. Norepinephrine is considered a second-tier choice and if considered, great attention must be paid to volume status in order to avoid precipitating systemic metabolic acidosis.

Guidelines 1. Methods of CSF Drainage • Two basic techniques of CSF drainage exist: intermittent and continuous. • Intermittent drainage for elevated ICP is the preferred method. When intermittent drainage is used, the opening and closing pressures and volume of CSF drained should be recorded, as this may give an indication of intracranial compliance. • Continuous CSF drainage at a specified pressure-height is an alternative, with the recognition that this method may interfere with continuous monitoring of ICP, unless an additional monitor is placed.

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2. Infection Control • Although there is some variation in practice, in general, empiric antibiotics will not be used for prophylaxis against infection after routine ICP monitor placement, including ventricular catheters. • Great attention will be paid to sterile placement and maintenance of ICP monitors, especially ventricular catheters, as conditions during placement and instrumentation are the greatest risks for inducing infection. • CSF will be sent for analysis from ventricular catheters as needed to rule out infection (e.g. after fever spikes, etc.). • CSF will be obtained using meticulous aseptic technique. • Only Neurosurgery team is allowed to obtain CSF from EVD or LSAD. • CSF catheter-ports will be sterilized with betadine and alcohol prior to instrumentation for obtaining CSF. • Intravenous broad-spectrum antibiotic regimen covering both Gram-positive and Gram-negative organisms will be initiated for treatment of suspected ICPmonitor infections. • Antibiotic regimen will be adjusted to conform to organism drug susceptibility. • Intrathecal antibiotics will be considered on a case-by-case basis.

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Sedation and Analgesia Background Sedation and analgesia in patients with severe head injury are important aspects of patient care that influence patient comfort, ability to tolerate mechanical ventilation and critical care procedures, and intracranial pressure management. The use of sedatives can improve ICP control, but may obscure the neurologic examination. Protocols for the use of sedatives in head injured patients vary widely, but most published series use significant doses of various agents including opiates, benzodiazepines, and propofol7, 8, 10. Many published protocols have also used prophylactic neuromuscular blockade5, 11. While the value of detailed serial neurologic examination in the patient with severe head injury (GCS 3-8) is debated, a sedation protocol that maximizes patient comfort, ICP control, and allows accurate neurologic examination is the ideal. Goals • • • Ensure patient comfort after severe head injury in the setting of critical care interventions. Serve as an adjunct for ICP management and perhaps to decrease secondary brain injury by decreasing cerebral oxygen utilization. Avoid interfering with clinical neurologic assessment as feasible.

Guidelines 1. Analgesia and Sedation are considered separate issues which must be addressed individually in each head injured patient. 2. Because sedation and paralysis are primary ICP-management modalities, any changes in sedation or paralytics in patients with ICP monitors must be cleared by the neurosurgery Chief Resident or Attending. 3. Analgesia • Patients will first be assessed for pain. • For pain management, initial doses to be considered are fentanyl 25-100 mcg IV q5-60’ or morphine 1-5 mg q30’-4o in bolus form. (Refer to 4E Analgesia and Sedation Guidelines for Adult ICU Patients, 1998 for more detailed dosage and dosing interval information.) • If initial attempts at analgesia are ineffective, then sedation (as described below) may be instituted. 4. Sedation in ICP Control • Sedation will be used in conjunction with other ICP control measures such as CSF drainage and mannitol. • Sedative usage will be avoided unless ICP remains elevated despite other ICP control measures, or unless needed to tolerate critical care interventions (e.g. mechanical ventilation, line placement, endotracheal suctioning, patient safety and restraint). • Propofol infusion at 10-100 mcg/kg/min is the preferred sedative. 25

Propofol will be tapered over 30 minutes QAM for morning rounds neurologic examinations and at other times when deemed necessary. • Triglyceride levels will be checked at baseline and every Monday with routine nutrition serology. If > 800, a lipase will be obtained and Propofol will be discontinued if this is elevated. • Alternative sedative infusions include benzodiazepines (midazolam, lorazepam) or opiates (morphine, fentanyl). These infusions may have less reliable offset than propofol, making neurologic assessment less reliable. • In patients receiving sedation, ongoing need for analgesia will be assessed and analgesia will be held if no indications of ongoing pain are present. 5. Neuromuscular Blockade • Neuromuscular blockade may be used in patients with severe head injury at the discretion of the treating physician. • Indications for usage include elevated ICP and severe pulmonary disease, such as ARDS. • Paralytics should be monitored with peripheral nerve stimulator to maintain at least 1 of 4 twitches, if tolerated. Atracurim and cisatracurium are alternatives to pancuronium and vecuronium in order to avoid concern of prolonged paralysis from impaired paralytic metabolism. • Sedative and/or opiate infusions will continue in all patients receiving neuromuscular blockade. •

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Hyperosmolar Therapy Background Mannitol is effective for treatment of elevated ICP after severe head injury. It is thought that an intact blood-brain barrier is necessary for maximal effectiveness of mannitol. Effects within minutes are observed due to rheologic effects on blood volume. Osmotic effects are seen within 15-30 minutes. Mannitol may be more effective when administered as intermittent boluses, rather than continuous infusion. Recent data also suggests that hypertonic saline solutions (3%, 7% or 23.4% NaCl) effectively reduce ICP. These solutions can be used as a primary treatment for increased ICP or as an adjunct to mannitol. Hypertonic saline (HTS) may also be effective as a salvage treatment in patients whom mannitol therapy has failed. Goals • • Treat acutely elevated ICP or diminished CPP, while avoiding hypovolemia. Treat clinical signs of cerebral herniation prior to ICP monitoring or if ICP does not reflect focal tissue shifts (e.g. focal temporal lobe pathology).

Guidelines 1. Mannitol dosing – 0.25-1.0 gm/kg as needed; consideration may be given to regular interval dosing (Q6 hrs), but continuous infusions will, in general be avoided. 2. Serum osmolarity should be kept below 320 mOsm, esp. if renal failure is a concern. 3. A suggested regimen is to check serum osmolarity 1 hour after prior mannitol dose. 4. Fluid replacement, usually with NS, will be undertaken to maintain appropriate volume status, usually euvolemia, as indicated in Section V. 5. Hypertonic saline solutions (3%, 7% or 23.4% NaCl) may be used at the discretion of the treating physician. 6. Plasmalyte is an alternative fluid replacement solution, especially in patients with metabolic acidosis (which may be exacerbated by large volumes of NS or HTS).

Guidelines 1. Barbiturate therapy may be considered in patients with persistently elevated ICP, especially if CPP remains diminished, despite maximal medical and surgical treatment, which usually includes CSF drainage, mannitol therapy, sedation +/paralysis, and mild hyperventilation. Consideration can be given to earlier institution of barbiturates in individual situations. 2. Barbiturate therapy consists of pentobarbital with a loading and maintenance dose • Loading dose: 10mg/kg over 30 minutes or 5 mg/kg Qhr x 3 • Maintenance dose: Initially 1 mg/kg/hr, adjusted Qhr based on ICP and EEG 3. Monitoring with EEG for burst-suppression is mandatory. • Initial interburst interval = 10-15 seconds, modify based on ICP control. • Pentobarbital loading should not be delayed for EEG placement. 4. Pulmonary-artery (PA) catheter placement may be useful. • Pressor and inotropic support are usually needed for patients undergoing barbiturate therapy. See Section V. • Pentobarbital loading should not be delayed for PA catheter placement. 5. Weaning of pentobarbital infusion, initiate after 24 hours of acceptable ICP control. • Decrease pentobarbital dose by 50% each day. • Discontinue pentobarbital 48 hours after wean initiated, if tolerated. • In individual situations, more rapid weaning of pentobarbital infusion may be considered, as tolerated.

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Hypothermia Background Hyperthermia, even of 1-2o C, worsens brain injury after experimental trauma. Hyperthermia is thought to worsen secondary brain injury after stroke, intracranial hemorrhage, and trauma in patients as well. Hypothermia has been considered as a neuroprotective strategy in all of these diseases. Presumably, hypothermia (usually to 32-33o C) decreases cerebral oxygen utilization and acts as a neuroprotectant. Despite reports from small series of improved outcome after induced hypothermia5, larger clinical trials have not consistently shown benefit. Also, there are concerns about systemic effects of hypothermia including coagulopathy, increased infection risks, and cardiac arrhythmias. At present, a strategy of avoiding hyperthermia is essential, with the role of induced hypothermia being less certain. Goals • • Avoid hyperthermia-induced secondary brain injury. Consider induced hypothermia as a 2nd or 3rd tier therapy for refractory elevated ICP.

Guidelines 1. Goal temperature (measured intravascularly or rectally) will be 35.5-37.0o C. 2. For T > 37.5o C, antipyretics such as acetaminophen will be initiated. 3. Mechanical measures such as cooling blankets and fans will be used to keep T < 37.5o C. 4. Appropriate measures will be taken to identify and treat infectious sources. 5. Around the clock antipyretics will be considered for patients with recurrent fever spikes. 6. Patients with shivering from fever or hypothermia measures will be treated as needed, per Sedation and Analgesia Guidelines. 7. Although intermittent doses of demerol (12.5-50 mg) may be considered for rigors/shivering in patients who cannot tolerate propofol, in general, demerol is to be avoided because of concerns that it may lower seizure threshold. 8. More aggressive hypothermia to 32-33o C using nasogastric lavage may be considered in cases of refractory elevated ICP.

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Glucocorticoids Background Glucocorticoids have been used in the past for treatment of brain edema in a variety of conditions, including head trauma, stroke, brain tumor, and cerebral abscess. Although currently used for vasogenic edema in tumor and abscess, they have been shown as ineffective in lowering ICP or improving outcome in patients with head trauma and stroke. Goals • • • Avoid use of steroids following TBI If steroids used as per Spinal Cord Injury protocols, monitor blood glucose and consider IV insulin drips for tight sugar control. Remain consistent with current literature and recommendations.

Guidelines 1. Glucocorticoids will not be used for the treatment of head trauma. 2. Glucocorticoid treatment for other indications may be provided in patients with head trauma. These indications include: • Concurrent spinal cord trauma. • Other conditions requiring corticosteroids (e.g. asthma, prior outpatient corticosteroid use). • In patients with head trauma who are receiving glucocorticoids for other indications, insulin infusion will be used to maintain serum glucose from 100200. • In patients with head trauma who are receiving glucocorticoids for other indications, non-depolarizing neuromuscular blocking agents will be avoided if at all possible, because of concerns of persistent paralysis from muscle damage induced by the combination of the two agents.

Guidelines 1. Based on physician discretion, patients with severe TBI requiring an ICP monitor may have one, or more, brain tissue monitors and microdialysis catheters to assess the brain tissue oxygen levels and cerebral metabolism. The protocol for placement and management is detailed in appendix 3. 2. Based on physician discretion, patients with ICP monitors may have jugular bulb catheters placed to help determine mixed venous cerebral oxygen extraction, and metabolic state. The protocol for placement and monitoring is outlined in appendix 4. 3. Based on physician discretion, some patients may also have parenchymal CBF monitors placed as part of the metabolic monitoring array. 4. Based on physician discretion, patients with severe TBI may have 24-hour electrophysiological (EEG) monitoring started as close to admission to the ICU as possible. MEP, SSEP, BAER, and P300 responses may also be evaluated at regular intervals. Electrophysiological monitoring and assessment will continue until it is deemed no longer necessary by the Neurosurgery attending in consultation with the neurocritical care team. 5. Based on physician discretion, patients will have CT perfusion scans and MR perfusion/diffusion scans as needed for quantitative and qualitative determination of cerebral blood flow and perfusion.

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6. Based on physician discretion, MR spectroscopy may be obtained as needed to determine the patients cerebral metabolic picture as a function of neuroanatomical geography. 7. Based on physician discretion, patients in whom diffuse axonal injury (DAI) is suspected may have an anatomical MRI and DTI to evaluate the integrity of the white matter tracts.

Seizure Prophylaxis Background Posttraumatic seizures may occur early, within 7 days of injury, or late, after 7 days. Seizures may worsen ICP control and worsen secondary brain injury, especially if status epilepticus occurs. Prospective, randomized trials have shown that prophylactic anticonvulsants may prevent the occurrence of early, but not late posttraumatic seizures12. Goals • Prevent early post-traumatic seizures.

Guidelines 1. After head injury, phenytoin (IV load 17 mg/kg and initial maintenance 100 mg IV TID or QID) will be instituted. 2. Fosphenytoin as a loading agent is preferred as hypotension may be less prominent. Intravenous preparations of loading and maintenance (fos)phenytoin are preferred as NG preparations may have less reliable absorption. 3. A phenytoin level will be obtained on day two. 4. Carbamazepine or phenobarbital will be considered if phenytoin cannot be tolerated. 5. In general, prophylactic anticonvulsants will be discontinued after seven days. 6. Patients with evidence of early posttraumatic seizures will initially be treated with 7 days of phenytoin then converted to Keppra 1500mg BID for a total of 6 months of therapy.

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Timing of Non-Neurosurgical Operative Procedures Background Patients with severe head injury often have other injuries which require operative intervention. Strategies designed to treat non-neurologic injuries may be at odds with the guidelines for management of severe head injury if hypovolemia or hypotension is tolerated. Issues related to non-neurosurgical operative procedures may exacerbate secondary brain injury if attention is not taken to avoid hypotension and aggressive volume resuscitation, especially with hypotonic fluids. Goals • Allow safe and successful treatment non-neurologic injuries, while avoiding secondary brain injury.

Guidelines 1. In general, neurologic management issues will take precedence in patients with severe head injury and multi-system trauma. 2. If a non-neurologic injury is immediately life-threatening, urgent medical and surgical intervention will be undertaken as appropriate, with attention to maintaining a minimum systolic BP > 90 mmHg (MAP > 90 mmHg strongly recommended) with volume and pressors, and PaO2 > 100 mmHg. ICP monitoring will be considered during the non-neurosurgical operative intervention with the threshold CPP of 70 mmHg being preferred. 3. For non-life threatening non-neurologic injuries requiring operative management, timing of surgery will be at the discretion of the Neurosurgery Attending, with input from the appropriate surgical service(s). In general, these procedures should be deferred until at least 1 week post-trauma. 4. Discussion will be undertaken between the surgical, neurosurgical, and anesthesia services prior to operative intervention in order in ensure accurate communication regarding goals of intra-operative neurologic management.

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Toxic/Metabolic Derangements Background TBI patients may experience significant toxic or metabolic derangements that may either alter their sensorium or affect their outcome. The most significant electrolyte abnormality associated with acute, post-traumatic neurological deterioration is related to shifts in serum sodium levels. Both hypo and hypernatremia are seen in the setting of TBI and both may cause alterations in mental status. Hyponatremia can result from iatrogenic causes (fluid overload) the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or cerebral salt wasting (CSW) syndrome. Hypernatremia can be due to the development of diabetes insipidus (DI) or may also be iatrogenic. Other metabolites frequently altered following TBI Cl-, Mg+, Ca+, and PO4-. Acid and base disturbances are also frequently seen in the TBI patient and may be due to respiratory or metabolic causes. Na+ Iatrogenic hypo and hypernatremia • Hyponatremia o Follows fluid overload o Associated with use of hypotonic crystalloid solutions • Hypernatremia o Associated with prolonged use of hypertonic saline solutions (3%, 7%, 23.4%) o Can cause hyperchloremia and associated metabolic acidosis. SIADH4; • Caused by release of Antidiuretic Hormone (ADH) in the absence of physiologic (osmotic) stimuli. • Results in hyponatremia (<134 mEq/L) with high urine osmolality (<280mOsm/L) • Usually accompanied by hypervolemia Cerebral Salt Wasting • The injured brain releases brain-derived natriuretic peptide • Renal sodium loss relults in hyponatremia and a decrease in extravascular volume4

ClHyperchloremia is frequently seen following aggressive hydration with either iso- or hypertonic saline solutions. Normal serum chloride levels range around 100 meq/dl compared to 154 meq/dl found in 0/9% NS. Increases in serum Chloride levels above 110 meq/dl can lead to renal loss of HCO3- and a subsequent metabolic acidosis. Mg++ Serum Mg++ levels vary widely and are often decreased following TBI – a condition linked to worsening outcome following TBI. Hypermagnesemia, though relatively rare following trauma, can be seen following massive tissue breakdown or in certain disease states such as renal failure, hypothyroidism and Addison’s disease. Numerous experimental brain injury models have demonstrated improved outcome, a decrease in cellular apoptosis and amelioration of diffuse axonal injury following Mg++ administration to maintain normal serum Mg++ levels. Administration of either MgSO4 of MagGluconate is easy, safe and effective for normalizing serum Mg++ levels.

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Ca++ Calcium abnormalities are frequently seen in the setting of large blood transfusions. As such, trauma patients are at risk for becoming hypocalcemic. Hypocalcemia itself may lead to cardiac dysfunction – particularly affecting cardiac contractility. The other major adverse effect of hypocalcemia is a coagulopathy. PO4Hypophosphatemia is relatively common following TBI. The degree of phosphate depletion can be quite severe and though the exact cause is not known, speculation centers around renal causes which may be exacerbated by use of mannitol. Given its role in Calcium metabolism, hypophosphatemia can cause calcium abnormalities, and its central role in energy metabolism explains its association with reduced intracellular 2,3-DPG and ATP levels. The latter abnormalities can be reversed with intravenous infusion of 6.8% potassium dihydrophosphate. Acid/Base Acid/base abnormalities are probably the most common metabolic disturbance seen in the TBI population. The immediate peri-traumatic period sees hypoperfusion from either excessive hemorrhage or from neurogenic hypotension as the most common causes. Drugs, ventilation abnormalities and chloride abnormalities (particularly hyperchloremia) may exacerbate acid/base imbalance while primary renal causes, chronic GI suctioning, and diarrhea will also affect serum pH. Of primary concern to neurosurgeon is the effect acid/base disturbances have on cerebral physiology. Intracranial hypertension can be difficult to manage in the face of an acidosis, due to the natural cerebral vasodilation to low pH. Conversely, a severe alkalosis may cause cerebral ischemia as cerebral vessels constrict. Goals • Early detection of metabolic abnormalities and identification of cause. • Performance of serial neurological examinations with interventions as necessary for correction of abnormality as well as treatment of confusion and agitation. Guidelines 1. Na+ • Hyponatremia: o First priority is to identify the cause of hyponatremia. Heading the differential are Cerebral Salt Wasting Syndrome (CSWS), SIADH and (iatrogenic) fluid overload – the main distinction between them being the patient’s volume status. In CSWS, patients are usually volume depleted whereas in both SIADH and fluid overload, patient’s intravascular volume is excessive.

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•

•

•

CVP measurements may be helpful in assessing volume status, though these may be difficult to interpret in patients on positive pressure ventilation with either high plateau pressure or PEEP readings. - Input/Output totals and daily weights are useful indicators of a patients volume status. - As a rule of thumb, CSWS tends to occur in the setting of ongoing brain injury and mainly in the early post-injury period. - Iatrogenic fluid overload should top the differential in patients who develop hyponatremia in a delayed fashion and in the absence of other ongoing injurious processes such as intracranial hypertension or meningitis. Cerebral Salt Wasting Syndrome o Suspect if hyponatremia develops in the early post-traumatic period. o Rx: - Ensure that maintenance IV solution is 0.9% NS. - Adjust to normalize CVP. - Begin 3% NaCl infusion at a rate of 30-50cc/hour. - Check serum Na+ every two to four hours – depending on degree of abnormality. - Hold infusion for serum Na+ ≥ 135 mmol/dl. - Consider active intracranial pathology (e.g. meningitis) if hyponatremia persistent or delayed in onset. - Consider SIADH/fluid overload if patient persistently hyponatremic. SIADH/Fluid Overload. o Consider fluid overload if initial resuscitation fluid is either half/quarternormal NaCl, P-lyte or LR. o Consider either if patient’s CVP is high or I/O net positive. o Rx: - Fluid restriction: between 1000-2000 cc/day – degree to be determined by severity of hyponatremia and volume status. - Check serum Na+ every two to four hours – depending on degree of abnormality. - In cases of unsuccessful fluid restriction, start with a 10% sodium correction in order to prevent neurologic sequelae4.  Stop if serum Na+ >126mEq/L over a period of 17+ 1 hours  Stop if the change in Na+ is > 10mEq/L in 24 hours - Do not exceed a rate of correction of 1.3 + 0.2mEq/L/hr - Second line therapy: NaCl tabs 3gms TID - If hyponatremia persists despite NaCl tab administration start 3% NaCl at 25-60cc/hr. - Consider active intracranial pathology (e.g. meningitis) if hyponatremia persistent or delayed in onset Hypernatremia o May result from excessive use of hypertonic saline solutions o Often used deliberately to decrease intracranial pressure (keeping serum Na+ 148-152 mmol/dl) o Usually inconsequential in the absence of Diabetes Insipidus (DI). 39

Infections Background TBI patients are at increased risk for infection. While some infections result from the trauma itself (e.g. open fractures, penetrating injuries), others are related to invasive procedures or other interventions (e.g. surgery, lines/catheters, intubation). The presence of severe neurologic dysfunction and need for heavy sedation and/or chemical paralysis further increase the risk of infection by decreasing patient mobility and impairing the ability to clear secretions. Finally, long hospitalizations, particularly within the ICU increase the risk of infection by organisms with multipledrug resistance. As such, prompt diagnosis and aggressive treatment of infections are imperative. Fever is the most common clinical presentation and may be associated with rigors, chills, tachycardia, tachypnea and in severe infections, hypotension. In the awake, unintubated patient, hyperventilation, disorientation and confusion may also be signs of a developing infection. Early laboratory findings include a rising white blood cell count, thrombocytsis, an elevated SED rate and a high C-reactive protein. One must keep in mind that these findings may be blunted in the in the elderly, immune compromised patients and in patients with an impaired thermoregulatory response. Posttraumatic meningitis occurs in 1-20% of patients with moderate to severe head injuries1. Most cases occur within two weeks of injury3. The most likely organisms are S. aures, Enterobacteriaceae, Pseudomonas sp., pneumococci4. Classic symptoms for meningitis include; o Headache o Fever o Sensorial disturbances o Neck and back stiffness o Positive Kerning sign o Positive Brudzinski’s sign o CSF abnormalities Goals • • • Early detection and work-up of potential infections processes. Involvement of General Medicine and Infectious Disease services when appropriate. Culture guided antibiotics with an identifiable duration of treatment.

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Guidelines 1. For temperatures > 38.5 oC, obtain pan culture to include sputum, urine, blood, and when appropriate CSF. 2. CXR to rule out presence of a respiratory source, when appropriate. 3. Duplex ultrasound evaluation in the presence of fever and swollen or tender extremity, to rule out DVT as a potential source. 4. Antibiotic coverage tailored to bacteriologic isolates and their sensitivities 5. Maintain euthermia (T ≤ 37.5 oC) using either surface or intravascular cooling techniques as required. 6. Repeat cultures every 48 hours if patient continues to have fevers. 7. Consider drug fevers or central hyperthermia in the setting of persistent fevers with multiple negative cultures 8. Consider obtaining an Infectious Disease consult.

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Drugs Background In patients with acute change in mentation, drug-induced encephalopathies must be considered. Many frequently used drugs (narcotics, benzodiazepines, tricyclic antidepressants, anticonvulsants, etc.) may cause an alteration in neurological status especially in the setting of TBI. (See cognition and behavioral guidelines) Goals • • Early identification of neurological altering substances. Minimize the use of neurological altering medications in the TBI patient population.

Guidelines 1. Pharmacological review for Central Nervous System (CNS) affects of medications prior to administration. 2. Follow Cognitive and Behavioral guidelines for prescribing potentially problematic medications. 3. Daily review of all medications currently prescribed and administered to the TBI patient by the physicians and nurses. 4. Weekly review by the IDT of medications both prescribed and administered.

Guidelines 1. Obtain a STAT head CT in the presence of acute neurological decompensation. 2. Consider adding a CTA to the study of a post-traumatic aneurysm suspected and the patient stable enough to tolerate the delay to the OR. 3. If a hematoma is present: a. Immediate neurosurgical evacuation where appropriate • ICP monitoring and treatment if not already instituted • Obtain coagulation panel • Consider repeat CT within 4-6 hours if the risk of recurrent or evolving hematomas considered a possibility

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Pain Management Background Inadequate pain management has been associated with poor outcome.Psychological and physiologic response to pain may produce profound pathophysiologic effects, these include sympathetic hyperactivity, vasoconstriction with increased blood pressure, tachycardia, regional ischemia, poor wound healing, hypoventilation, atelectasis, hypoxemia and thromboembolic complications Pain assessment and management in the post-traumatic head injured patient is complex, as it must be instituted during, and in association with the ongoing diagnostic evaluation of the extent of neurological injury. Altered mental status, impaired cognition and communication may make patient self-report of pain an unavailable assessment tool. The IDT may be required to utilize biological markers, such as heart rate, blood pressure, respiratory rate and behaviors, as key assessments in the TBI patient. Goals • Pain management in the TBI patient is directed toward providing adequate patient comfort for compliance with diagnostic assessment and rehabilitation efforts while maintaining physiologic/hemodynamic stability and providing minimal CNS related side effects.

Clinical Guidelines – Medical Management
Location ED Responsible Party MD Intervention NSU Team
Interns – first response, must contact Chief Resident. at time of ED call Chief Resident – must personally see patient in ED or CT for GCS < 12 Attending – must attend all surgical procedures. Must review all consults within 30 minutes if in-house. Must see all overnight consults on AM (0600) rounds.

Clinical Guidelines– Medical Management
Location LHH Responsible Party MD MD/NP/Nurse MD/NP Intervention Daily medical management to be provided by accepting MD Neurosurgery clinic appointments to be scheduled at the time of discharge from the acute care setting. Additional SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Prior to discharge from LHH The patient and family will be instructed to report to the ED for emergencies They will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise. SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Patient and family members will be instructed to report to the ED for emergencies. Patient and family members will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise. SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Patient and family members will be instructed to report to the ED for emergencies. Patient and family members will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise.

III. Nutritional Management
Background TBI patients exhibit moderate to severe hypermetabolism immediately following trauma. Energy expenditure has been reported as 75% to 250% of basal energy expenditure. Caloric requirements are directly related to motor activity, infection, fever, level of sedation, level of consciousness, alterations in ICP, and any additional injuries. TBI patients can remain hypermetabolic and hypercatabolic from 1 week to 1 year post-injury. Enteral or parenteral nutrition support is often required and should begin as soon as the patient is hemodynamically stable. When clinically feasible, enteral nutrition should be used since it offers economic and physiologic benefits without severe complications. If enteral nutrition is contraindicated because of nonfunctioning gastrointestinal tract, parenteral nutrition can be utilized. Nutrition intervention is necessary for optimal recovery of the TBI patient. Goals • • • Provide adequate kilocalories and protein to prevent extensive muscle catabolism and to improve nitrogen balance Maintain tolerance to nutrition therapy. Reconsult nutrition as needed to address problems promptly. Follow patient per department protocol (See Screening Process for Clinical Nuturition – Appendix B-1).

IV. Cognitive Dysfunction
BACKGROUND Patients sustaining a traumatic brain injury may exhibit a broad range of cognitive deficits. The Glascow Coma Scale (GCS) and the Rancho Los Amigos Scale of Cognitive Functioning are two scales commonly used to assess the depth of coma, the severity of the head trauma, monitor changes in the patient’s status and make predictions regarding outcomes. (See Appendices C-1 and C-2 for scale descriptions) These scales are used by members of the interdisciplinary team (IDT) to consistently describe the patient at the time of onset, throughout recovery and to measure progress. These patients often exhibit reduced safety awareness as well as reduced awareness of the implications of their deficits, which manifests in unsafe and occasionally aggressive behavior. GOALS • • • • Provide a safe therapeutic environment Improve patient/caregiver knowledge of cognitive deficits and compensatory strategies to reduce agitation and facilitate ongoing functional improvement. Improve and maximize cognitive functioning. Address behavioral issues while considering their current Rancho Level.

GUIDELINES 1. Assessment • All disciplines will screen the patient for cognitive deficits. Informal assessment methods are used for patients functioning at Rancho Levels IIV. Assessment consists of the IDT observing the patient in a natural environment, as well as in response to various stimuli. All staff may make observations regarding a patient’s level of arousal/attention, ability to verbalize, localization to sound, and response to tactile, auditory and olfactory stimulation. Responses should be documented and used to determine the current Rancho Level. Any deterioration of mental status will be reported immediately to the primary physician. • Formal/Standardized assessment may be initiated when a patient is functioning at Rancho Level V. Assessment is completed by the Speech Pathologist and/or the Neuropsychologist. While a patient at this level is still confused, he/she is following commands inconsistently, is less agitated and better able to participate. Common areas of impairment which will be addressed in a cognitive-communicative evaluation are: o Disorientation o Memory impairment o Reduced attention to task o Visuospatial/perceptual deficits o Problem solving/verbal reasoning impairmen 56

2. Treatment • Once the assessment has been completed, and the Rancho Level has been determined, therapy is initiated. The goals of treatment and the techniques used to manage the cognitively impaired patient vary according to their level of functioning. Therapy addresses the impairments noted during the evaluation as they affect basic and community level activities. Patient/caregiver education is a crucial part of the recovery process, and must occur at every level. The IDT will provide ongoing teaching to the caregivers and family, with both written and verbal instruction, regarding cognitive deficits specific to the patient and suggestions to maximize cognitive function and reduce agitation. (See Appendix? for Patient/Caregiver Education Materials) Instructions for interacting with the patient will be placed at the bedside to ensure an optimal environment for recovery. These instructions will be dependent on the patient’s level of functioning. (See Appendix?) o Rancho Levels I-II: - At this stage, the patient is either completely unresponsive or reacting inconsistently to stimuli in a non-specific manner. - All members of the IDT should:  Simplify, structure and heighten stimuli to produce ever increasing levels and frequency of motor responses, beginning with the patient localizing the stimulus, without causing disruption in the patient’s homeostasis  Supply each stimulus with an intended motor response that is verbally requested or implied by the therapist’s handling of the patien  As the patient responds more consistently, channel his/her responses into more appropriate interaction with the environment  Increase level of responsiveness to all sensory stimulation. Stimulation Therapy  The goal of stimulation therapy is to increase the patient’s response to the environment. (See Appendix C3 for SFGH Sensory Stimulation Program)  When indicated, this therapy is typically performed by the family, in coordination with a Speech Pathologist and other members of the IDT.

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o Rancho Levels III-IV: - When localization is present, such as the patient pulling on a nasogastric tube, catheter or resisting restraints, all members of the IDT should attempt to:  Obtain greater consistency in localizing responses and avoiding stereotypic movements  Decrease interval between stimulation and response See Appendices C3 and C4  Increase the patient’s ability to follow simple commands, attend to an activity, and use common objects, such as a spoon  Identify more precisely motor or sensory impairments by observing bed positioning, periods of restlessness, and facial responses  Continue to increase the consistency, variety and quality of stimuli  Decrease agitation  Increase cognition and perception  Reduce stimuli that increases agitation and increase situations that calm the patient  Focus the patient’s attention on the external environment, by engaging him/her in self care activities and other automatic tasks  Remove restraints during periods of supervision, such as therapy sessions  Provide structure and predictability in the daily routing to reduce confusion  Soothe the patient by rocking, warm, sustained touch, slow vestibular stimulation, tapes of familiar voices, talking with the patient, physical activity such as walking or being wheeled, and other repetitive techniques o Rancho Level V-VI: - When the patient’s agitation decreases, he/she will respond more to the external environment, at first in confused and inappropriate ways. As the response may become more appropriate, there continues to be poor short-term memory, difficulty learning new tasks, persistent confusion, decreased attention, visual-spatial dysfunction, dyspraxia, and/or inconsistent orientation. The Speech Pathologist, as well as other members of the IDT perform cognitive therapy. Therapy may be hampered by the patient’s irritability, lack of cooperation, mood fluctuations, impulsivity, ease of frustration, dependence on the family, confusion, and disorientation. - Goals of therapy at this level are to:  Increase attention to more specific tasks  Increase process of sequential organization  Increase immediate and short-term memory  Increase analysis, association and categorization skills

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Staff should continue to:  Structure the patient’s environment  Reduce complexity and duration of tasks to the patient’s ability  Keep distractions to a minimum  Change immediate environment and schedule as little as possible o Rancho Level VII: - When the patient demonstrates fairly consistent responses to the external environment, the goals are to:  Decrease the external structuring of the patient’s environment gradually  Increase the patient’s purposeful goal-directed behavior  Increase initiation of independent living and daily skills  Increase performance of more complex tasks  Increase responsibility for tasks and consequences  Increase awareness of physical and cognitive limitations  Improve the patient’s cognitive and social skills - Cognitive Remediation:  Focuses on increasing the patient’s ability to concentrate on specific tasks, organize and use information, remember increasing amounts of information and be mentally flexible. It includes systematic use of activities to develop skills, repeated practice by the patient, selection and teaching of compensatory cognitive methods and cueing strategies, as well as constant systematic feedback. - Tasks include:  Complex reading and mathematical tasks  Tasks involving increasing analysis of information, such as summarizing paragraphs, interpreting stories etc.  Money management tasks  Deductive reasoning tasks  Sequencing cards, word scrambles, map reading, jigsaw puzzles, board games, card games, computer programs and planning and preparing for social activities, such as a trip into the community. - Safety  The Rehabilitation Service will assist the IDT in assessing the patient’s safety/safety awareness. This will include issues regarding restraint use, supervision in the prevention of falls, elopement and assaultive behavior, as well as optimal environment for recovery 3. Post Traumatic Amnesia (PTA) • Anterograde Amnesia o Anterograde amnesia is the inability to form consistent day-to-day memories secondary to a brain injury. o Damage to the brain usually occurs in one of three areas; the hippocampus, basal forebrain or the diencephalon. o Symptoms: 59

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- Disorientation to person, place, and/or time - Confusion and agitation - Decreased attention span - Short term memory deficits - (Long term memory remaining intact) - Compromised ability to learn new information o The use of cognitive testing can assist it in determining specific areas of deficit. To maximize cognitive recovery, therapy should focus on acquisition of new skills through repetition within the defined attention span. • Retrograde Amnesia o Retrograde amnesia is the inability to remember occurrences prior to and including the injuring event. o As the patient recovers, memories leading up to the traumatic event may return. However, many patients never regain memory of the actual injuring incidence. In recovery, improvement from retrograde amnesia typically follows resolution of anterograde amnesia. 4. Stress Disorders • Acute Stress Disorder (ASD) o Acute Stress Disorder is and anxiety disorder that develops within one month after a severe traumatic incident. Symptoms can effect any sex or age group and include; - Distressing dissociative symptoms - Depersonalization - Derealization - Dissociative amnesia - Anxiety - Irritability - Depression - Diminished ability to experience pleasure - Problems falling or staying asleep o Patients with acute stress disorder will avoid any reminders of the trauma and frequently relive the event in the form of dreams, nightmares, or painful memories. As a result of the above symptoms the patient suffering from acute stress disorder may be misdiagnosed as having cognitive deficits and behavioral issues. • Posttraumatic Stress Disorder (PTS) o Posttraumatic stress disorder is a result of exposure to a traumatic event, to oneself or surrounding others, in which he/she experiences intense fear, horror, or a sense of helplessness. The experience must involve a threat of death, serious injury, or threat to physical integrity. o The individual usually suffers from one or more of the following disociative symptoms; - Loss of emotion, numbing, or detachment - Diminished awareness of surroundings - Depersonalization - Derealization - Dissociative amnesia 60

o The event is often re-experienced in one of the following ways; - Distressing recollections of the event or experience - Dreams that are reoccurring and distressful - Reliving the event or experience in the form of flashbacks, - hallucinations, images, illusions, or thoughts - Reacting in a physiological manner to any aspect of the event or - experience o Symptoms of PTS are like those of an acute stress disorder but also include; avoidance of any thing associated with the trauma (i.e. thoughts or feelings about the incident, and a refusal to engage in conversation about the event). The patient will frequently avoid activities, places, persons, or things he/she associates with the traumatic experience. o For a diagnosis of PTS symptoms must persist longer than 4 weeks following the incident. o It is the responsibility of the interdisciplinary team to possess a heightened awareness of such disorders and seek evaluation and intervention by psychiatric services. Early screening and acute symptom management will aide in the recovery process.

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V. Behavioral Management
Background TBI patients often exhibit cognitive and behavioral dysfunction either as a result of their injury or from a pre-existing/pre-injury condition. Deficits may include memory loss, difficulty with executive function, reduced safety awareness, emotional liability, social disinhibition, agitation or impulsivity. Moreover, their presence and severity may vary over time and in an unpredictable fashion. Because of this, reassessment must be frequent and treatment adaptable to changing patient conditions. The interplay between cognitive dysfunction and behavioral issues is complex and their interdependence can complicate patient management. For example, patients may have short term memory loss in addition to reduced safety awareness and lack of insight. As such, their inability to understand the implications of their deficits combined with their inability to remember instructions may lead to unsafe situations. This may lead to the imposition of behavioral limits by hospital staff – a situation that may unintentionally increase patient frustration and possibly lead to aggressive behavior. In order to avoid a cycle of increasingly stricter limits culminating in physical restraints and sedation, therapeutic strategies should rather re-direct patient behavior and diffuse situations that might otherwise escalate. These strategies should address a patient’s emotional state and cognitive limitations and focus on optimizing physical environment and personal interactions and minimizing the use of psychoactive medications. Finally, frequent re-assessment is needed to adapt therapy to the patient’s changing neurological function. In the acute setting of severe TBI, the Glasgow Coma Score (See GCS - Appendix C-1) is useful for assessing neurological function. However, for patients with less severe injury (or for those emerging from coma) the Rancho Los Amigos (RLA) Scale of Cognitive Functioning (Appendix C-2) is more useful and is the basis for the following set of guidelines. Goals • • • • • • • To optimize patient function through early cognitive/behavioral intervention To provide a ward environment that minimizes patient agitation and conducive to learning To minimize the use of physical restraints To minimize the use of psychoactive medications To include both patient and family in the rehabilitation process through education and involvement in the treatment plan, with particular attention to behavioral issues and management. To develop a Interdisciplinary team (IDT) approach to cognitive and behavioral dysfunction in patients with TBI To establish protocols detailing the manner and frequency of cognitive/behavioral assessment 62

• •

To establish protocols for disseminating information amongst the appropriate clinical services To build performance improvement systems within the guidelines

Guidelines 1. Cognitive Evaluation (Please refer to section on cognitive dysfunction) 2. Cognitive Treatment Guidelines (Please refer to section on cognitive dysfunction) 3. Behavioral Evaluation • The Interdisciplinary Team (IDT) must evaluate maladaptive behaviors (e.g., agitation, pulling tubes, attempting to climb out of bed, striking out) during the weekly IDT case conference, and more frequently, if needed. A focused progress note outlining the evaluation of the problem and plan for intervention should include: o Identification of the behavior to be modified. o Identification of the triggers leading to the behavior (This may include who might trigger the behavior, what situations trigger the behavior, and what environmental conditions are present when the behavior occurs.). o Identification of the treatment goal (e.g., decrease fall risk, limit agitation, decrease striking out.) o Determination of a plan for intervention and implementation (This should include assignment of roles to IDT members.) o Determination of a follow up date to evaluate success of intervention(s) used (The follow-up date may be the next IDT case conference, or at an earlier date, as needed.) 4. Behavioral Interventions • Agitation o Excessive restlessness, often associated with over-stimulation or mental distress. - Acknowledge the patient’s discomfort and reassure him of your desire to help. - Address the patient in a calm and soothing manner. - Keep the lights low in the room. - Turn the TV off in periods of agitation. - Keep statement simple and concise when addressing the patient. Detailed explanations or instructions tend to increase the patient’s agitation. - Limit the number of people in the room; step out of the room to address others. • Combativeness o Striking out intentionally or unintentionally - Maintain your awareness of your position relative to the patient. Stand back to avoid being hit or kicked. Do not crowd the patient; give the patient his “space.” - Address the patient in a calm and soothing manner. - Acknowledge the patient’s discomfort. - Let the patient know that you will be calling for additional help if needed. 63

Avoid backing self into a corner when leaving the room. Always keep your back facing the patient. - If possible, remove any objects that may potentially harm the patient. • Impulsivity o The tendency to become active suddenly and spontaneously without planning the activity or thinking about the consequences of the actions. - Always assess the environment for safety before asking the patient to initiate an activity. - Inform the patient in a gentle but firm manner at the time an unsafe or impulsive behavior is observed. Call attention to the consequences. Suggest alternative behaviors. - Maintain spatial distance when setting limits until a sense of the patient’s response is obtained. - Cue the patient to slow down and think out loud before responding. - Orient patient to use of call light. 5. Psychopharmacological Interventions • Psychotropic interventions play a role in facilitating the recovery process through such areas as limiting agitation, improving attention and concentration, or promoting regular sleep-wake cycles. However, with any use of psychotropic medications, as with the use of restraints, the risks and benefits of its use must be weighed. 6. Safety Evaluation • The nursing service will assist the IDT in assessing in the patient’s safety/safety awareness. This will include issues regarding restraint use, supervision in the prevention of falls, elopement and assaultive behavior, as well as engineering the optimal environment for recovery to reduce the presence of potentially hazardous objects. Institutional police should be called if the patient is violent and a threat to him/herself or others or if uncontrolled escalating behavior develops. IDT members should instruct the institutional police in management of the patient. 7. Safety Intervention • Physical Restraints o Definition: Please refer to the Policy and Procedure 18.9 regarding restraint use. o Types: - Based on the definition of physical restraints, the following items are considered restraints:  Wrist and ankle restraints  Mitts  Waist restraints  Vests (Poseys)  Vail beds o Use: - While the use of a restraint is often initiated to protect intravenous sites or tubes or decrease risk of fall, utilization of a restraint is not without risk. Examples of injuries related to restraint use may include, but are not limited to, entanglement, pressure ulcers, or fractures related to falls caused by climbing over a side rail. A full assessment by the IDT 64

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•

of the risks and benefits of restraint use will be assessed weekly at the IDT meeting. The risks and benefits must also be discussed with the patient’s family; documentation of such discussion must be evident in the medical record. - Careful monitoring (as per Nursing policy) of the use of the restraint, its efficacy, and ongoing behaviors necessitating its continued use must be documented. Discussion of the need to continue use of the restraint must be discussed at the weekly IDT meetings or more frequently, as needed. Environmental Interventions o For all TBI patients, limiting excessive environmental stimulation is crucial. Consideration of the environment may also be helpful in both limiting future behavioral problems as well as facilitating the recovery process. As a patient recovers, a gradual increase in the degree of stimulation that a patient receives may begin, for example, by introducing exposure to light and other elements of his surrounding. This may assist him in becoming more aware of day and night, and staff and family members, thereby improving orientation and sleep. The following Stimulation Precautions may be posted to assist family, friends, and staff in providing the degree of stimulation appropriate for a patient’s level of recovery. o Environmental Stimulation Precautions: Please see Appendix C-4.

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Behavioral: Symptom Evaluation and Intervention
Symptom Anxiety and Agitation Evaluation Before using any medication to treat anxiety and/or agitation felt to be due primarily to the TBI, other diagnoses that may result in such behavior must be ruled out. This includes evaluation for the presence of metabolic dysfunction, sympathetic hyperactivity, thyroid disease, drug or alcohol withdrawal, or any pre-morbid psychiatric illness, physical discomfort, thirst, hunger, constipation, oxygen desaturation . Eliminate medications that may exacerbate anxiety, if possible. These medications may include benzodiazepines, certain SSRIs, antidepressants, narcotics, albuterol, and H2 blockers. Evaluate for the presence of situational or environmental factors that might contribute to increased anxiety and intervene accordingly. Such factors may include limiting overstimulation, assessing if particular visitors incite increased anxiety, and developing a regular toileting program. Medications While minimizing agitation and/or anxiety is the goal, caution should be exercised in the administration of these medications to avoid over sedation. Worsening of the patient’s mental status due to over sedation may mask the presence of a true neurological decline or confound the neurologic examination, thus necessitating a neurologic work up. Further, over sedation limits the patient’s ability to safely participate in therapies and attend to tasks. Any neuroleptic may result in tardive dyskinesia or neuroleptic malignant syndrome. AIMS testing when appropriate to rule out dystonia. Monitor medications for possible paradoxical effects such as agitation. Anxiety / Agitation Related to Drug Benzodiazepines such as lorazepam and Withdrawal diazepam may be of benefit, but presents the risks of negative side effects, including excess sedation and adverse effect on cognition. Anxiety / Agitation Not Related to Drug If a sleep disturbance is felt to be contributing to Withdrawal the patient’s level of anxiety. Consult with psychiatry for drug choice and dosing. Low doses of Trazadone may be initiated and increased until nighttime sleep is achieved. Anticonvulsants (e.g., tegretol and valproic acid) have demonstrated benefit in the control of agitation. Imminent Danger to Self/Others or Judicious use of short-acting benzodiazepines or Agitation Limiting Ability to Render neuroleptic agents may be helpful in these cases. Medical Care Agitation Associated With Inattention or Stimulants (e.g., methylphenidate and amantidine) Distractibility have been useful in these instances. These medications have also been helpful in patients who demonstrate a lack of initiation, mimicking depression, with respect to participating in tasks. Agitation Associated With Sympathetic Beta blockers may be utilized in this setting, when Hyperarousal other etiologies for the symptoms of sympathetic hyperarousal are ruled out. Of note, beta blockers may cause CNS side effects (e.g., nightmares, hallucinations, and insomnia) and may be contraindicated in patients with COPD and diabetes.

Anxiety and Agitation (Continued)

66

Behavioral: Symptom Evaluation and Intervention
Symptom Anxiety and Agitation (Continued) Agitation Related to Anxiety Agitation Related to Psychotic Symptoms, Including Delusions, Hypervigilance, and Hallucinations Sleep Disturbance Buspirone has been used with some success in this setting. Of note, buspirone has demonstrated little sedative effect or adverse impact on cognition. Respiradol may be considered. Respiradol has minimal central nervous system effects, such as sedation, as compared to other psychotropic medications.

Evaluation Use of a sleep chart can be helpful in tracking for the presence of a sleep disturbance. This may include checking the patient at intervals of 30 minutes. Evaluate for the presence of situational or environmental factors that may adversely affect the patient’s sleep patterns. This may include noise within the room or hallway, or frequent medically-related interventions (e.g., vital signs, neurochecks, respiratory treatments). Evaluate for physiologically-related factors that may affect sleep. These factors may include posttraumatic stress disorder, sleep apnea, premorbid history of insomnia, or age >60 years.

Medications The goals of therapy should be to assist in re-establishing the sleep/wake cycle. Different medications affect the sleep cycle in different ways; certain agents may be selected base on these interactions. All are not without potential side effects that may be adversely affect a patient’s recovery. Antidepressants: Trazadone increases slow wave sleep and improved REM sleep latency. Amitryptiline may increase total sleep time, improve sleep quality, and decrease number of awakenings. Anticholinergic Psychosis is a frequent complication of antidepressant administration Benzodiazepines (“Middle Acting”): Clonazepam may decrease the number of awakenings and increase Stage 4 sleep. Abrupt withdrawal may result in seizure or death. The side effects of paranoia may complicate recovery process. Sedation, anterograde amnesia, impaired motor performance with increase risk of falls, paradoxic agitation, and abuse potential are side effects inherent to all benzodiazepines. Hypnotics: Ambien, Restoril have been shown to assist with sleep. Sedation and impaired motor performance are risk factors that need to be considered. Based on information from the Behavior Management Program, Policy and Procedure Manual, Santa Clara Valley Medical Center, and on Pharmacology and Brain Rehabilitation, Physical Medicine and Rehabilitation Clinics of North America, 8:4, November 1997.

Interdisciplinary discussion of cognitive, behavioral, and psychiatric issues
Weekly plan for cognitive rehabilitation tract Medication and restraint re-assessment Psychiatric Evaluation When: Prior history of psychiatric disorder Behavioral problems refractory to environmental control Rehabilitation program to be adapted to current Rancho Los Amigos level of cognitive functioning. Referral to outpatient ST as indicated Outpatient ST for continued cognitive therapy as indicated Rehabilitation program to be adapted to current Rancho level.

Guidelines 1. Rehabilitation Referral Process in the Acute Setting • Early assessment and intervention by Rehabilitation Services (Physical Therapy, Occupational Therapy, Speech Therapy, Physiatry) is critical in the treatment of TBI patients to facilitate early improvement and to prevent complications. 2. General Assessment and Treatment • Comprehensive evaluation of the TBI patient is crucial in the development of treatment plans. Rehabilitation Services will identify the need for, and facilitate planning of, ongoing interventions. Assessment will include identification of a patient’s premorbid status in order to develop realistic treatment goals. All assessments will include: o Tone - Physical interventions may include positioning, splinting, and/or neuromuscular techniques for inhibition/facilitation to normalize tone

73

Medical interventions will be considered when increased spasticity limits function. Interventions may include initiation of baclofen, tizanidine, dantrolene, and/or benzodiazipines. Baseline and follow-up laboratory evaluations may be necessary, depending on the agent used. Botulinum toxin injections or motor point blocks if a more focused approach to a particular joint is needed. o Strength/Motor Control - Muscle control and or strength will be assessed by observation, handling or Rood scales if spasticity is present. Scales of zero to five (0-5) or zero to normal will be used for patients who do not exhibit spasticity. Neuromuscular facilitation techniques to maximize return of strength/motor control will be employed. A therapeutic exercise program will be developed for each patient to address his or her individual needs. - TBI patients who are medically paralyzed and/or sedated, or who have sustained motor impairments as a result of their injury, are at risk for pressure sores due to immobility. The use of multipodus splints, specialized mattresses or beds, specialized wheelchair cushions, and/or special positioning programs may be recommended by Rehabilitation Services in the prevention of pressure sore formation. o Range of Motion (ROM) - ROM measurements will be performed and documented. A therapeutic exercise program will be developed to prevent ROM deficits and contractures, and to maximize functional ROM. This may include use of splinting or special positioning programs to maintain functional ROM. - Heterotopic ossification (HO) may result in significant losses of ROM that may adversely affect function. Special attention must be paid to any warm, painful joint, even if the joint has no apparent relation to the patient’s injuries. Initial evaluations may include plain films of the affected joints (although this may be insensitive to early HO), and/or triple phase bone scan. Alkaline phosphatase may be elevated in patients with HO, however, alkaline phosphatase may often be elevated in TBI patients for other co-morbid conditions. Treatment is controversial and may include active or active-assisted ROM and the use of didronel. In the late stages of HO (often when the bone scan is negative), surgical excision may be considered. o Activities of Daily Living (ADL’s) - Assessment of ADL functions will be performed with each patient. The assessment will include:  Basic ADL’s:  Dressing  Grooming  Feeding  Bathing  Toileting  Mobility (transfers, wheelchairs)  Ambulation (residence) 74

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o Cognitive Skills (Please also refer to Cognitive Guidelines) - Mental flexibility - Executive functioning - Problem-solving o Community-Level ADL’s for community reintegration: - Safety awareness/judgement for household and community level activities - Medication management - Community-level visual/perceptual skills o Financial management - Basic Community Life Skills (i.e. keeping appointments, managing transportation) - A treatment plan will be developed and implemented for each patient based on their individual needs to maximize or improve ability to perform basic community ADL’s in an independent-as-possible manner. Appropriate assistive devices will be obtained for each patient to maximize functioning. Such equipment may include selffeeding utensils, sock aides, commode, transfer bench, medisets, etc. o Mobility - Assessment of mobility will be performed on each patient. A therapeutic program will be developed and implemented for each patient based on their individual specialized needs. The following levels of mobility will be assessed:  Bed mobility (scooting, rolling, sidelying to sit)  Transfers (Bed-to-wheelchair, wheelchair-to-toilet, wheelchair-tobath, wheelchair-to-mat, car)  Wheelchair mobility (level surfaces, community surfaces, on to buses, and into taxi’s)  Gait (household, community, with/without distractions, level/uneven surfaces, curbs, ramps, stairs, hills) - Appropriate assistive devices will be obtained for each patient to maximize functional mobility. These may include orthotics, walking aides, specialized wheelchairs, and wheelchair cushions. o Dysphagia - When appropriate, Speech Therapy (ST) will evaluate patients to determine if swallowing is within functional limits. ST will recommend appropriate diet levels, and/or recommend tube feedings, if appropriate, to ensure adequate nutrition and safety. Recommendations will be made regarding the level of supervision needed at mealtimes and any compensatory techniques necessary to facilitate safe swallowing. ST may recommend video fluoroscopy for detailed evaluation of the patient’s ability to swallow, if indicated.

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o Activity level for Nursing/Staff Assistance - Each component of the Rehabilitation team’s assessment will include a plan with therapeutic interventions to maximize function. The plan may include instructions to nursing staff to assist the patient in an appropriate and safe manner when the level of assistance for safe mobility/activity does not require the skilled intervention of the rehabilitation team. Specific instructions will be provided to the nursing staff, specific to each patient.

Guidelines 1. Positioning • A positioning program should be implemented early in the TBI patient’s course of treatment, to be implemented by all members of the IDT who may be involved in any physical manipulation of the patient. In addition to the IDT staff members, this also includes the TBI patient’s family and friends. • Proper positioning is critical in the prevention of: o Contractures. o Abnormal patterns of muscle tone. o Dysfunctional postures and positions of the head, trunk and pelvis, particularly: o Abnormally forward head. o Protracted and forward scapula. o Posterior pelvic tilt. o Trunk tightness. • Positioning in Bed o Sidelying (or semiprone) is preferable to supine o Head: neutral, aligned with spine. o Bottom upper extremity: scapular protraction, humeral external rotation, and flexed to approximately 90 degrees; elbow is flexed. o Top upper extremity: scapular protraction and slight shoulder flexion, resting on a pillow, and elbow is extended. o Wrists: with use of splinting, maintain wrist in extension, maintain palmar space. o Lower extremities: pillow between knees, and under lower leg, if needed, to maintain alignment with the thigh and to prevent pressure sores; flex knee and hips slightly. o If supine position required: - Shoulders: place small pillow underneath scapula, shoulders in slight abduction and external rotation. - Upper extremities: elbows extended, splinting for wrist extension and finger splinting. - Lower extremities: slight knee flexion with the use of pillows.

NDT and PNF o Both methods may be combined with quick stretch, tapping over the muscle belly and joint approximation. o Quick ice can be applied to the muscle belly or for directionality of motion on flaccid muscles.

Work toward: o Channeling the patient’s responsiveness and alertness. o Increasing the patient’s ability to move independently and begin to participate in activities of daily living.

Guidelines 1. Neuromuscular Treatment • Utilizing NDT, PNF, or other techniques in the facilitation of specific muscles, introduce mat activities to elicit head and neck control, rolling, and sitting. Neuromuscular techniques can also be utilized in facilitating transitional movement, such as moving from prone to prone-on-elbows, or from prone to sidely, etc. 2. Perception and Cognition • (See Cognitive and Behavioral Guidelines) 3. Agitation • (See Cognitive and Behavioral Guidelines) RLA Level V–VI Rehabilitation Characteristics RLA V: Patients at this level demonstrate localization as a response to stimulation. The responses are quicker and more appropriate, such as pushing away a painful stimulus, visual tracking, and blinking in response to a bright light. RLA VI: Patients at this level demonstrate responses to stimulation that is more appropriate, such as withdrawing from stimuli that is noxious or irritating, but not to stimuli that produces no discomfort. Patients are able to carry out simple requests and initiate purposeful activity. Rehabilitation Interventions Goals • As the patient’s agitation decreases, he will respond more to the external environment, initially confused and responding in inappropriate ways. Other deficits will become more evident, including: poor short-term memory, difficulty learning new tasks, persistent confusion, decreased attention, visual-spatial dysfunction, dyspraxia, and/or inconsistent orientation. Given this, the goals are to: o Increase: - Attention to tasks and specific stimuli. - Process of sequential organization. - Immediate and short-term memory. - Analysis, association and categorization of tasks. 81

Intubated
PT/OT/ST consult. Early ROM. OOB to chair Communication regarding daily plan of care to be provided via written notes, verbal communication with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education.

Extubated
PT/OT/ST consult. ROM and progressive mobilization. Transfer training. Activities of daily living. ST swallow and cognitive evaluation (see nutrition and cognition pathways). Communication regarding daily plan of care to be provided via written notes, verbal communication with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education. Rehabilitation program to be adapted to current Rancho level. Communication regarding daily plan of care to be provided via way of written chart notes, verbal contact with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education. Acute rehabilitation program per accepting MD and based upon current Rancho level. Initiate referrals for needed outpatient rehabilitation services. Continue outpatient rehabilitation services. Vocation rehabilitation and re-training programs. Continue outpatient rehabilitation services. Vocational rehabilitation and re-training programs. Nurse Practitioner: NP Speech Therapy: ST Physical Therapy: PT

VI. Substance Abuse
Background Studies of the prevalence of alcohol use disorders in trauma patients have shown elevated rates compared to community populations. Studies of the prevalence of drug use disorders in trauma patients are minimal. In other medical conditions, the presence of a substance use disorder is associated with poorer outcomes, a more complicated course of treatment, increased utilization, decreased quality of life and functionality and decreased treatment compliance. There are several studies that document that TBI patients with substance use disorders follow a similar pattern of medical complications. Goals • • • • Detect and manage substance withdrawal Educate patient and family about substance use disorders and their interaction with TBI Support patient through the use of motivational interviewing and by facilitating attendance at appropriate patient support groups Promote integrated treatment of substance use disorders at all levels of care

Guidelines 1. Detection and management of substance withdrawal • A team effort to gather substance use history from collateral sources and laboratory information is necessary to screen for the risk of substance withdrawal, as the patient may not be able to provide a complete history. • Substance withdrawal will be included in the differential diagnosis of TBI patients with at risk substance use who develop agitation and/or delirium. • Patient and family education • Culturally appropriate patient and family education materials on substance use disorders will be available. • Team members will have an adequate knowledge of the interaction of substance use disorders and TBI, so that the patient will have multiple brief educational interventions. 2. Patient Support • Team members will be knowledgeable about patient support and twelve step programs available to hospitalized patients. • Team members will be knowledgeable of facilitation techniques for support and twelve step programs. • Team members will be knowledgeable about motivational interviewing techniques to facilitate patient discussions about substance use. • Integrated Treatment of Substance Use Disorders • On site treatment for patients with substance use disorders will be available at all levels of care. • Community referrals for TBI patients with substance use disorders will be performed when patients are ready for discharge. 86

Clinical Guidelines – Substance Abuse Location
ED

Responsible Party
MD/NP MD/NP/Nursing

Intervention
Neurological exam History Drug use Alcohol use Prior withdrawal Cognitive, behavioral, or psychiatric disorders Medications Drug and alcohol toxicology screen N/A Anesthesia notification of drug and alcohol history and positive toxicology Intubated Obtain drug and alcohol history from family, including prior history of withdraw symptoms Monitor for signs and symptoms of withdrawal Thiamine, Folate, and Multivitamins Alcohol management with propofol and beta blockers Extubated Obtain drug and alcohol history from family including prior history of withdrawal symptoms Monitor for signs and symptoms of withdrawal (See Appendix D-1) Thiamine, Folate, and Multivitamins Detox. management per CIWA guidelines (See Appendix D-2) Continue Thiamine, Folate, and Multivitamins Continue to monitor for signs and symptoms of withdrawal (See Appendix D-1) Detox. management per CIWA guidelines (See Appendix D-2) Substance Abuse Service consultation Drug and alcohol counseling and program initiation Enrollment in drug and alcohol rehabilitation program Community drug and alcohol counseling and meetings Community counseling and meetings

VIII. Patient and Family Education and Psychosocial Support
Background A wide body of literature has demonstrated that comprehensive patient and family education, and psychosocial support improves health outcomes: quality of care, satisfaction, cost efficiency and most importantly, patient and family adjustment to life altering illness. Consistent with the mission and vision of San Francisco General Hospital, Patient / Family and psychosocial support education is delivered to all patients in a culturally, educationally and linguistically appropriate manner. Goals • To provide an effective, coordinated, and integrated education and psychosocial support protocol for the TBI population and their families. The plan embraces comprehensive, interdisciplinary and collaborative patient and family education and psychosocial support throughout the recovery continuum. The educational and patient/family support process recognizes that patients and their families are an integral part of treatment and goal setting.

Guidelines 1. It is the responsibility of all Interdisciplinary Team (IDT) members to assess the readiness of patients and families for educational content and the need for family support. The educational plan will be individualized and based upon the IDT assessment. SFGH patient education documentation standards will be followed (SFGH P&P 5.14, Nursing P&P 11.2- Addendum II Interdisciplinary Patient Education Record): 2. The Social Worker will conduct an ongoing psychosocial assessment of family coping and needs including the grieving process, practical and emotional support systems, coping skills, and financial resources (SFGH P&P 1.17,sec. IV). IDT will monitor changes in coping and family needs throughout the recovery continuum, adapt the treatment plan and make necessary referrals. 3. Patient/Family educational barriers, preferences, motivation and stressors will be assessed by all IDT members upon admission and at regular intervals throughout the hospital stay. Family and patient educational resources include the TBI library located on 4B and the Patient Education Resource Center (PERC) located in the medical Library. These services include on-line access, SFGH TBI Program link, and materials developed specifically for the TBI population. 4. The IDT will assess for educational readiness for the T.B.I. patient utilizing the Rancho Los Amigos Scale of Cognitive Functioning. The family will be educated at each stage of functioning. Family will be included in goal setting. 5. Interdisciplinary rounds will include the development of an individualized educational care plan for each patient/family. IDT members are responsible for educational content pertaining to their individual disciplines for both the family and T.B.I. patient. Individualized educational materials will be determined by patient condition and provided along the recovery spectrum. 88

6. Patient and family centered care meetings may be called by any member of the IDT for coordination of the recovery process, educational issues, family support, and development of a comprehensive discharge plan. The IDT will meet prior to discuss the patient’s status and to appoint a “team leader” for the family meeting. 7. Evaluation of financial resources for the patient and family are an integral component of treatment planning and family education. The eligibility worker explores these resources, verifies insurance coverage and distributes pertinent information to the Social Worker and the Utilization Review Nurse. If the patient does not have coverage, and is eligible for Medi-Cal, the eligibility worker will refer to the Medi-Cal worker who will assist the Patient/family in the completion of the application. Should the patient also need monetary assistance, the Social Worker will assist with applications to SDI, SSI, or General Assistance (GA). The SFGH SSI worker may be consulted to assist the SW with new applications or verification of existing cases. Medical insurers are contacted and kept appraised of patient’s ongoing recovery, level of care, medical and rehabilitation needs by the Utilization Review Nurse. 8. IDT will assess patient’s readiness for discharge as determined by medical stability, functional ability, fiscal resources and family input. A collaborative effort by the IDT is made to determine a viable discharge plan. The Patient or surrogate is educated about options for rehabilitation needs, and is the ultimate decision-maker. The MS will arrange transportation and discharge referrals. The IDT will support the family during the decision making process and through the transition to the appropriate level of care.

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Clinical Guidelines - Education and Psychosocial Support
Location Responsible Party
Social Work IDT

Intervention
Early patient identification, family contact, and supportive counseling. Give patient status updates, provide education for diagnostic work-up, patient admission status, notification of chaplain services, or family support network as requested. N/A Assist family in obtaining medical updates Early social work consultation, crisis intervention, and support. Patient identification and family contact if not already established, obtain contact number. Begin psychosocial assessment as appropriate. Begin discharge planning Identify social issues and impediments to discharge plan Initiate all transfers when appropriate (including rehabilitation) Assist to identify family needs for coping and education. Family education and orientation to the ICU, individualize educational materials based upon family assessment and readiness. IDT to establish the educational plan on IDT rounds. Investigate/verify health insurance coverage. Obtain contact person and benefit coverage. Initiate health insurance application as appropriate. Complete necessary portion of LHH referral.

ED

Radiology OR ICU

Social Work Social Work

IDT

Eligibility

Assess level of care for patients on an on-going basis. Maintain regular contact with health insurance case manager. Assist in LHH/4A referrals and in transfers.

4B

Utilization Review Social Work

Continue psychosocial evaluation or begin assessment as appropriate Continue discharge planning Include family in goal setting. Family to be educated at each stage of functioning. IDT responsible for educational content pertaining to their discipline. Coordinate education plan along care continuum. Assess patient and family preferences, motivation, and stressors. Refer to TBI library and P.E.R.C. Patient educational readiness to be determined by RLA scale Coordinate family centered care meetings. Provide family updates regarding discharge plan. Co-coordinate weekly interdisciplinary rounds. Initiate referrals to in-house resources, financial assistance programs, and to community services.

IDT IDT

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Clinical Guidelines – Patient and Family Education and Psychosocial Support
Location
Discharge to Community from SFGH or LHH

Responsible Party
IDT

Intervention
Assess patient’s readiness for discharge; to be determined by medical stability, functional capacity, family input, and fiscal resources. Provide referrals for TBI support groups Explore home environment and identify impediments to discharge. Clarify funding for necessary outpatient rehabilitation services and home equipment. Coordination with LHH and Department of Public Housing (pending) Coordination with LHH and Department of Public Housing (pending)

TBI Clinical Guidelines: ICU Clinical Guideline
Mobility Responsible Party Intervention
Intubated PT/OT/ST consult. Early ROM, bed mobility, therapeutic exercise. OOB to chair Communication regarding daily plan of care to be provided via written notes, verbal communication with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education. Extubated PT/OT/ST consult if not previously obtained. ROM and progressive mobilization. Functional transfers. Gait training Activities of daily living. Swallow and cognitive evaluation(see nutrition and cognition pathways). Communication regarding daily plan of care to be provided via written notes, verbal communication with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education. Intubated Obtain drug and alcohol history from family, including prior history of withdraw symptoms Monitor for signs and symptoms of withdrawal Thiamine, Folate, and Multivitamins Alcohol management with propofol and beta blockers Extubated Obtain drug and alcohol history from family including prior history of withdrawal symptoms Monitor for signs and symptoms of withdrawal (See Appendix D-1) Thiamine, Folate, and Multivitamins Detox. management per CIWA guidelines(See Appendix D-2)

Intervention
Rehabilitation program to be adapted to current Rancho level. Communication regarding daily plan of care to be provided via way of written chart notes, verbal contact with the primary team, and the IDT board. Weekly plan of care to be discussed at IDT rounds. Family training and education. Continue Thiamine, Folate, and Multivitamins Continue to monitor for signs and symptoms of withdrawal (See Appendix D-1) Detox. management per CIWA guidelines (See Appendix D-2) Substance Abuse Service consultation Continue psychosocial evaluation or begin assessment as appropriate Continue discharge planning Include family in goal setting. Family to be educated at each stage of functioning. IDT responsible for educational content pertaining to their discipline. Coordinate education plan along care continuum. Assess patient and family preferences, motivation, and stressors. Refer to TBI library and P.E.R.C. Patient educational readiness to be determined by RLA scale Coordinate family centered care meetings. Provide family updates regarding discharge plan. Co-coordinate weekly interdisciplinary rounds. Initiate referrals to in-house resources, financial assistance programs, and to community services.

Substance Abuse

Education and Support

MD/NP MD/NP/Nursing MD/NP MD/NP/Nursing Substance Abuse Service Social Work

TBI Clinical Guidelines: LHH Clinical Guideline
Medical Responsible Party MD MD/NP/Nurse MD/NP Intervention Daily medical management to be provided by accepting MD Neurosurgery clinic appointments to be scheduled at the time of discharge from the acute care setting. Additional SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Prior to discharge from LHH The patient and family will be instructed to report to the ED for emergencies They will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise. Continue current nutritional guidelines Diet advancement based upon swallow progression as determined by ongoing ST evaluation Rehabilitation program to be adapted to current Rancho Los Amigos level of cognitive functioning. Referral to outpatient ST as indicated

Evaluate intervention success Outpatient Neuropsychology evaluation and treatment as indicated
Acute rehabilitation program per accepting MD and based upon current Rancho level. Initiate referrals for needed outpatient rehabilitation services. Drug and alcohol counseling and program initiation Assess patient’s readiness for discharge; to be determined by medical stability, functional capacity, family input, and fiscal resources. Provide referrals for TBI support groups Explore home environment and identify impediments to discharge. Clarify funding for necessary outpatient rehabilitation services and home equipment.

Intervention
SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Patient and family members will be instructed to report to the ED for emergencies. Patient and family members will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise. Continue current nutritional guidelines Diet advancement based upon swallow progression as determined by ongoing ST evaluation Outpatient ST for continued cognitive therapy as indicated Identify behavior to be modified Agitation Combativeness Impulsivity Identify behavioral triggers Environmental Implement Environmental interventions Behavioral interventions Psychotropic interventions Evaluate intervention success Outpatient Neuropsychology evaluation and treatment as indicated Continue outpatient rehabilitation services. Vocation rehabilitation and re-training programs.

Medical

Nutrition Cognition Behavior

ST ST

Mobility

Neuropsychology PT/OT/ST

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TBI Clinical Guidelines: Transitional Housing

Clinical Guidelines Substance Abuse Education and Support

Responsible Party
Social Work

Intervention
Enrollment in drug and alcohol rehabilitation program Community drug and alcohol counseling and meetings Coordination with LHH and Department of Public Housing (pending)

Intervention
SFGH neurosurgery clinic appointments to be scheduled at the discretion of the SFGH Neurosurgery Service and prior to next visit. Patient and family members will be instructed to report to the ED for emergencies. Patient and family members will be provided with a direct contact number for the neurosurgery clinic, should questions or complications arise. Continue current nutritional guidelines Diet advancement based upon swallow progression as determined by ongoing ST evaluation Identify behavior to be modified Agitation Combativeness Impulsivity Identify behavioral triggers Environmental Implement Environmental interventions Behavioral interventions Psychotropic interventions Evaluate intervention success Outpatient Neuropsychology evaluation and treatment as indicated Continue outpatient rehabilitation services. Vocational rehabilitation and re-training programs. Community counseling and meetings Coordination with LHH and Department of Public Housing (pending)